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目的： 探讨正常钾浓度尼可地尔灌注液致心脏停搏作用及其对未成熟心肌缺血－再灌注损伤的保护作用． 方法：采用幼兔（３周龄～４周龄）离体工作心模型，分别以Ｓｔ．Ｔｈｏｍ ａｓ Ⅱ液、冷血停搏液及尼可地尔停搏液（依次为Ⅰ，Ⅱ，Ⅲ组）经主动脉灌注使心脏停搏，在缺血前及缺血后记录心电活动情况、心功能、心肌肌浆网Ｃａ２＋ －ＡＴＰａｓｅ 活性及心肌超微结构变化． 结果： ①尼可地尔灌注液（１．６ ｍ ｍ ｏｌ／Ｌ）可致未成熟心肌电－机械活动静止，复灌后有满意复跳． ②Ⅲ组心功能恢复率明显优于Ⅰ，Ⅱ组（Ｐ＜ ０．０５）． ③Ⅲ组心肌酶ＣＰＫ活性明显小于Ⅰ组（Ｐ＜ ０．０５）． ④Ⅱ，Ⅲ组心肌肌浆网Ｃａ２＋ －ＡＴＰａｓｅ活性明显高于Ⅰ组（Ｐ＜ ０．０１）． ⑤电镜下心肌超微结构显示Ⅲ组优于Ⅰ，Ⅱ组． 结论： 尼可地尔（１．６ ｍ ｍ ｏｌ／Ｌ）灌注液可致未成熟心肌电－机械活动静止，其心肌保护作用明显优于传统的Ｓｔ． Ｔｈｏｍ ａｓ Ⅱ冷停搏液，与冷血停搏法相比有更好的趋势．
Objective: To investigate the cardiac arrest caused by normal potassium concentration nicorandil perfusion and its protective effect on immature myocardial ischemia-reperfusion injury. Methods: The isolated heart model of young rabbits (3 weeks to 4 weeks old) Thom as Ⅱ liquid, cold blood cardioplegia and Nicorandil cardioplegia (followed by Ⅰ, Ⅱ, Ⅲ group) by aortic perfusion to cardiac arrest, ECG recording before and after ischemia, Cardiac Function, Cardiac Sarcoplasmic Reticulum Ca2 + -ATPase Activity and Myocardial Ultrastructure Changes. Results: (1) Nicorandil perfusion solution (1.6 m mol / L) induced immature cardiomyocyte electromechanical activity at rest. ② The recovery rate of cardiac function in group Ⅲ was significantly better than that in group Ⅰ and Ⅱ (P <0.05). ③ The activity of CPK in group Ⅲ was significantly lower than that in group Ⅰ (P <0.05). ④ The activity of Ca2 + -ATPase in myocardial sarcoplasmic reticulum in group Ⅱ and Ⅲ was significantly higher than that in group Ⅰ (P <0.01). ⑤ Electron microscopy myocardial ultrastructure showed that group Ⅲ was superior to group Ⅰ and Ⅱ. CONCLUSION: Nicorandil (1.6 m mol / L) perfusate can cause immature myocardial electromechanical activity quiescence, its myocardial protective effect is significantly better than the traditional St. Thom as Ⅱ cold cardioplegia, compared with the cold-blooded carding method has a better trend.